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Ciliary neurotrophic factor (CNTF) is primarily known for its important cellular effects within the nervous system.

However, recent studies indicate that its receptor can be highly expressed in denervated skeletal muscle.

Finally, PD98059, a specific inhibitor of p44/p42 MAPK pathway, was able to abolish the effects of CNTF on both myoblast fate and MRF expression.

Our results demonstrate the myogenic lineage-committed human myoblasts can dedifferentiate at a clonal level and CNTF is a novel regulator of skeletal myoblast dedifferentiation via p44/p42 MAPK pathway. Myoblast fate is critically dependent on the myogenic regulatory factors (MRFs): Myo D, Myf5, myogenin, and Mrf4, which have a well-defined role in orchestrating skeletal muscle development and differentiation.

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Here, we investigated the direct effect of CNTF on skeletal myoblasts of adult human.

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After removal of all fleas the study was repeated and the contact between cats lasted 48 h.

The total numbers of fleas recovered out of the 600 fleas deposited on the 6 donor cats after each infestation were 499 and 486 at 24 h and 48 h respectively.

These “progenitor cells” retained their myogenic memory and were capable of redifferentiating into myotubes.

Furthermore, CNTF could activate the p44/p42 MAPK and down-regulate the expression of myogenic regulatory factors (MRFs).

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